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Biomedical subjects

H C Lin

Publications and source records attributed to H C Lin.

At least 19 recordsLinked to original sources
PubMed1997

Phosphatidylinositol (4,5)-bisphosphate-dependent activation of dynamins I and II lacking the proline/arginine-rich domains.

Dynamins comprise a family of GTPases that participate in the early stages of endocytosis. The GTPase activity of neuronal specific dynamin I is stimulated by microtubules, negatively charged phospholipid vesicles, and Src homology 3-containing proteins, including Grb2. These activators were previously shown to bind to a proline/arginine-rich domain (PRD) in the carboxyl-terminal region of the enzyme. Dynamin II, which is ubiquitously expressed, had not been purified or characterized previously. In this study, the enzymatic properties of rat dynamin II and of D746, a dynamin II truncation mutant lacking the PRD, have been characterized. Dynamin II has a higher basal activity than dynamin I, but the two types of dynamin are stimulated similarly by microtubules, Grb2, and phospholipids. D746 is not activated by microtubules or Grb2, highlighting the significance of the PRD for these interactions, but it is activated by phospholipid vesicles containing phosphatidylserine or phosphatidylinositol-4,5- bisphosphate. Moreover, in contrast to previous reports, the PRD appears not to be required for phospholipid-stimulated self-assembly of dynamin, which is a key element in the regulation of its activity. Similar results were obtained with bovine brain dynamin I that had been subjected to limited proteolytic digestion to remove the PRD. Our data highlight the potential involvement of dynamin pleckstrin homology domains in the regulation of GTPase activity by phospholipids.

Animals↗
PubMed1997

Use of xylazine, butorphanol, tiletamine-zolazepam, and isoflurane for induction and maintenance of anesthesia in ratites.

Anesthetic effects of xylazine, butorphanol, tiletamine-zolazepam, and isoflurane in ratites (9 emus, 3 rheas, 6 ostriches) were determined. Anesthetic treatments included 4 regimens: induction and maintenance of anesthesia with isoflurane, preanesthetic tranquilization with xylazine and butorphanol followed by induction and maintenance of anesthesia with isoflurane, induction of anesthesia with tiletamine-zolazepam and maintenance with isoflurane, and preanesthetic tranquilization with xylazine and butorphanol followed by induction of anesthesia with tiletamine-zolazepam and maintenance with isoflurane. None of the birds developed irreversible adverse effects, but 2 developed brady cardia (1 was treated with atropine and responded) and 2 others developed transient apnea. Intravenous administration of tiletamine-zolazepam produced rapid and smooth induction of anesthesia in adult ostriches.

Adjuvants, Anesthesia↗
PubMed1997

Inositol phosphate responses in portal veins from portal hypertensive rats: receptor- and nonreceptor-mediated responses.

BACKGROUND/AIMS: Venous hyporesponsiveness in portal hypertension has been reported previously by us. The present study was undertaken to investigate possible changes of phosphoinositide signal transduction pathway in the portal veins from portal hypertensive rats METHODS: Portal hypertension was induced by partial portal vein ligation. Fourteen days after surgery, portal veins were removed for measurement of [3H]inositol phosphate responses to both receptor- and nonreceptor-mediated stimuli. RESULTS: Basal [3H]inositol phosphate formation was similar between the two groups. Both phenylephrine and angiotensin II stimulated [3H]inositol phosphate formation in portal veins, but the responses were attenuated in the portal hypertensive group. In contrast, the [3H]inositol phosphate formation by nonreceptor-mediated stimuli (GTP gamma S, NaF/AlCl3, and phospholipase C) was similar between the two groups. CONCLUSION: Our results showed that the receptor-mediated [3H]inositol phosphate formation was attenuated, while the non-receptor-mediated formation was unaltered, in the portal vein from portal hypertensive rats.

Angiotensin II↗
PubMed1997

Aminoguanidine corrects hyperdynamic circulation without ameliorating portal hypertension and portal hypertensive gastropathy in anesthetized portal hypertensive rats.

BACKGROUND/AIMS: Portal hypertension and hyperdynamic circulation (i.e. generalized vasodilation and increased cardiac output and regional organ blood flows) may play an important role in the development of portal hypertensive gastropathy. This study investigated the effect of chronic administration of aminoguanidine, a selective inducible nitric oxide synthase inhibitor, to portal hypertensive rats on hemodynamics and the development of portal hypertensive gastropathy. METHODS: Partial portal vein-ligated or sham-operated rats were randomly assigned to receive either placebo (distilled water) or aminoguanidine (approximately 100 mg/kg per day subcutaneously) for 2 days prior to and 14 days. Hemodynamic studies with a thermodilution technique and gastric morphometric analysis were performed at 14 days after the operation. RESULTS: In rats given placebo, portal vein-ligated rats had a significantly lower mean arterial pressure and systemic vascular resistance associated with a significantly higher cardiac index and portal pressure than sham-operated rats (p<0.05). In portal vein-ligated rats aminoguanidine induced a significant increase in mean arterial pressure and systemic vascular resistance accompanied by a significant decrease in cardiac index (p<0.05) without changes in portal pressure (p>0.05). Despite persistence of portal hypertension, the aminoguanidine-treated portal vein-ligated rats had similar mean arterial pressure, cardiac index, and systemic vascular resistance as seen in placebo-treated sham-operated rats. The mean cross-sectional area of gastric mucosal vessels was significantly higher in placebo-treated portal vein-ligated than in placebo-treated sham-operated rats (p<0.05). Treatment with aminoguanidine did not induce changes in the mean cross-sectional area of gastric mucosal vessels in either portal vein-ligated or sham-operated rats (p>0.05). CONCLUSIONS: The results show that in portal hypertensive rats long-term aminoguanidine therapy corrects the hyperdynamic circulation without inducing changes in portal pressure and ameliorating the development of portal hypertensive gastropathy. This study suggests that, instead of correcting hyperdynamic circulation, treatment of portal hypertensive gastropathy should be aimed at reducing portal pressure.

Animals↗
PubMed1997

Comparison of cytokeratin fragment 19 (CYFRA 21-1), tissue polypeptide antigen (TPA) and carcinoembryonic antigen (CEA) as tumour markers in bronchogenic carcinoma.

To elevate the diagnostic value of the serum cytokeratin 19 fragment (CYFRA 21-1) and compare it with carcinoembryonic antigen (CEA) and tissue polypeptide antigen (TPA) in bronchogenic carcinoma, the sera of 161 patients (58 with benign pulmonary disease and 103 with bronchogenic carcinoma) was investigated using immunoradiometric assay. Sensitivities for CYFRA 21-1, CEA and TPA (using 3.5 ng ml-1, 5.0 ng ml-1, 110 U l-1, respectively, cut-off values corresponding to a 95% specificity for benign pulmonary disease) in bronchogenic carcinoma were 64, 47 and 61%, respectively. Positive CYFRA 21-1 levels were identified in 75% of patients with squamous cell carcinoma (n = 36), in 67% with adenocarcinoma (n = 45), in 17% with large cell carcinoma (n = 6), and in 50% with small cell lung cancer (SCLC) (n = 16). However, CYFRA 21-1 levels were not significantly different between squamous cell carcinoma and the other histological types. The sensitivity of the combined measurement of CYFRA 21-1 with any other tumour marker was significantly higher than that of CYFRA 21-1 measurement alone. Elevated CYFRA 21-1 levels were observed in 44% of Stages I and II (n = 18) and 72% of Stage III and IV (n = 69) patients with non-small cell lung cancer (P < 0.05). A significant inter-marker correlation was observed between CYFRA 21-1 and TPA (n = 103, r = 0.448, P < 0.0001). Twenty-one patients were monitored by CYFRA 21-1, and significantly different changes in progressive patients (P = 0.0058) and regressive patients (P = 0.016) were obtained. These results indicate that CYFRA 21-1 may be not only a sensitive tumour marker in the diagnosis of bronchogenic carcinoma, but also a useful marker for the monitoring of bronchogenic carcinoma.

Adenocarcinoma↗
PubMed1997

Characteristics of non-participants and reasons for non-participation in a population survey in Kin-Hu, Kinmen.

The aim was to characterize non-participants and to investigate reasons for non-participation in a health survey in Kin-Hu township, Kinmen, Republic of China. The non-participants represented 25.6% of the target population of 4,451 registered residents aged 30 and older. Baseline demographic characteristics and two-year mortality for the participants and non-participants were compared. A house-to-house visit was attempted to all of the non-participants for reasons of refusal. The mean age of the non-participants was significantly older than that of the participants (54.3 versus 48.5 years, p < 0.001). The response rate for women was significantly higher than that for men (77.2% versus 71.6%, p < 0.001). The probability of death was significantly different between the two groups (1.2% versus 8.8% for participants and non-participants, respectively, p < 0.001). Major reason for not having participated in the health survey was 'not notified or informed of the examination' (32.7%). These data suggest that non-participants were less healthy.

Adult↗
PubMed1997

Intestinal transit is more potently inhibited by fat in the distal (ileal brake) than in the proximal (jejunal brake) gut.

Fat in the proximal and distal gut inhibits intestinal transit as the jejunal brake and the ileal brake. It is unknown, however, whether the intestinal transit response to fat in the proximal vs distal gut is different. Since surgical removal of the distal small intestine induced faster transit and greater steatorrhea than removal of the proximal small intestine, we hypothesized that the ileal brake inhibited intestinal transit more potently than the jejunal brake. In six dogs equipped with duodenal (10 cm from pylorus) and midintestinal (160 cm from pylorus) fistulas, we compared intestinal transit across an isolated 150-cm test segment (between fistulas), while 0 (buffer), 15, 30, or 60 mM oleate was delivered into either the proximal (between fistulas) or the distal (beyond the midintestinal fistula) half of the gut. The half of the gut not receiving oleate was perfused with buffer. Buffer perfused into both the proximal and the distal half of the gut served as the control. A meal was administered and diverted completely out of the duodenal fistula so that the studies were all done in the fed state. Intestinal transit was measured by counting for the recovery of a radioactive marker from the temporarily diverted output of the midintestinal fistula. We found that (1) intestinal transit was inhibited more potently by oleate in the distal than in the proximal half of the gut (region effect; P < 0.01), (2) oleate inhibited intestinal transit in a load-dependent fashion (dose effect; P < 0.05), and (3) load-dependent inhibition of intestinal transit by oleate depended on the region of exposure (interaction between load and region; P < 0.01). We conclude that intestinal transit is more potently inhibited by fat-induced ileal than jejunal brake.

Animals↗
PubMed1997

Effect of endogenous nitric oxide on tumour necrosis factor-alpha-induced leukosequestration and IL-8 release in guinea-pigs airways in vivo.

1. Tumour necrosis factor-alpha (TNF-alpha) is implicated in the pathogenesis of many pulmonary and airway diseases. TNF-alpha stimulation may release interleukin-8 (IL-8) in airways mediated via an increase in intracellular oxidant stress. In the present study, we have assessed leukosequestration and IL-8 release in the airways in response to intratracheal administration of human recombinant TNF-alpha, and examined the modulatory role of endogenous NO by pretreatment with a NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME). 2. TNF-alpha (10(2)-10(-4) u) was administered intratracheally in male guinea-pigs which were anaesthetized with urethane and were ventilated artificially. TNF-alpha induced a time- and dose-related increase in neutrophil numbers and a concomitant increase in human IL-8 equivalent level retrieved from bronchoalveolar lavage (BAL) with the peak effect at 10(3) u at 6 h of TNF-alpha injection (late phase). Intratracheal administration of recombinant human (rh)IL-8 (0.025, 0.25, 2.5 ng) producing a similar range of human IL-8 equivalent levels in BAL as measured in our results induced neutrophil recovery in BAL fluid to a similar extent. Administration of anti-IL-8 antibody prevented the late phase of neutrophil recruitment induced by TNF-alpha or rhIL-8. 3. Pretreatment with L-NAME significantly enhanced the TNF-alpha (10(3) u)-induced neutrophil recruitment and human IL-8 equivalents production at 6 h, but not at 1 h of TNF-alpha administration (early phase). L-Arginine reversed the responses to L-NAME. Pretreatment with 0.2% DMSO (i.v.) significantly inhibited TNF-alpha-induced neutrophil recruitment and human IL-8 equivalents release both in the early and late phase of the responses. Pretreatment with DMSO also inhibited the enhancement effect of L-NAME on the late phase of TNF-alpha-induced responses. DMSO failed to modify exogenous rhIL-8-induced neutrophil recruitment. Neither L-NAME nor DMSO alone induced any significant change in neutrophil numbers or human IL-8 equivalent level in BAL fluid. 4. Neutrophil depletion by cyclophosphamide pretreatment failed to modify TNF-alpha-induced human IL-8 equivalent release. 5. The expression of beta 2-integrin, CD11b/CD18 on neutrophils was increased only in the late but not early phase of TNF-alpha stimulation. L-NAME failed to modify these responses. 6. In conclusion, we demonstrated that NO may be an important endogenous inhibitor of TNF-alpha-induced leukocyte chemotaxis via inhibition of IL-8 production. Thus, the production of NO in airway inflammatory diseases may play a negative feedback role in self-limiting the magnitude of inflammatory responses.

Animals↗
PubMed1997

Hyperdynamic circulation of cirrhotic rats with ascites: role of endotoxin, tumour necrosis factor-alpha and nitric oxide.

1. Hyperdynamic circulation observed in portal hypertensive states is characterized by generalized vasodilation, increased cardiac index and increased systemic and regional blood flows. Endotoxin, tumour necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) have been reported to be involved in the pathogenesis of hyperdynamic circulation, but the interactions between endotoxin, TNF-alpha and NO in cirrhotic rats with ascites have never been specifically addressed. 2. This study was designed to determine systemic and portal haemodynamics and plasma levels of endotoxin, TNF-alpha and nitrate/nitrite in cirrhotic rats with ascites and investigate the relationships between these substances. 3. Plasma concentrations of endotoxin, TNF-alpha and nitrate/nitrite (an index of NO production) were determined in 25 cirrhotic rats with ascites and 17 control rats using the Limulus assay, ELISA and a colorimetric assay respectively. In addition, haemodynamic studies were performed in another ten cirrhotic rats with ascites and ten control rats. 4. Cirrhotic rats with ascites had hyperdynamic circulation accompanied by increased plasma levels of endotoxin, TNF-alpha and nitrate/nitrite, as compared with control rats. Significant correlation existed between plasma levels of endotoxin and nitrate/ nitrite (r = 0.59, P < 0.0001) and between plasma levels of endotoxin and TNF-alpha (r = 0.63, P < 0.0001). No correlation was detected between plasma levels of TNF-alpha and nitrate/nitrite (r = 0.24, P > 0.05). 5. This study suggests that endotoxaemia developed in cirrhotic rats with ascites may stimulate NO formation directly or indirectly via cytokine cascade, and consequently participate in the development and/or maintenance of hyperdynamic circulation.

Animals↗
PubMed1997

Chronic administration of propranolol improves vascular contractile responsiveness in portal hypertensive rats.

Propranolol is used clinically as a prophylactic drug to prevent oesophageal variceal bleeding in cirrhotic patients with portal hypertension. Vascular hyporesponsiveness is a common characteristic of the portal hypertensive state. The present study aimed to investigate whether chronic administration of propranolol could improve vascular responsiveness in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL). Sham-operated rats served as controls. There were four study groups: PVL-propranolol group (portal hypertensive rats receiving propranolol), PVL-vehicle group (portal hypertensive rats receiving saline), sham-propranolol group (sham-operated rats receiving propranolol) and sham-vehicle group (sham-operated rats receiving saline). Propranolol (30 mg kg-1 day-1) or saline was given for 9 days via gastric gavage starting 1 day before ligation and thereafter. Then, the superior mesenteric artery was removed from each group for contractile study after haemodynamic measurement. In portal hypertensive rats, propranolol significantly alleviated the hyperdynamic state, including portal pressure, cardiac index and total peripheral resistance in the treated group compared with the vehicle group. The maximal contractile responses to KCl and vasopressin in mesenteric artery were significantly greater in the sham-vehicle group than in the PVL-vehicle group. Long-term propranolol treatment enhanced the contractile reactivity of mesenteric artery to KCl and vasopressin in PVL rats, and the contractile profiles were corrected towards those in sham-treated animals. In contrast, propranolol treatment decreased heart rate, mean arterial pressure and cardiac index but did not alter the contractile responsiveness of sham-operated rats. These results showed that, in portal vein stenosed rats, long-term treatment with propranolol improved arterial contractile reactivity together with portal pressure reduction. The propranolol effect on vascular reactivity is probably related to haemodynamic improvement, instead of a direct contractile effect on the vasculature.

Animals↗
PubMed1997

Fiber-supplemented enteral formula slows intestinal transit by intensifying inhibitory feedback from the distal gut.

Because an increase in flow rate accelerates intestinal transit, a reduction in the flow rate of formula delivery is recommended frequently for treatment of diarrhea that develops during enteral feeding. Because intestinal transit is slowed by nutrient-triggered inhibitory feedback, the rate of intestinal transit during enteral feeding may depend on a balance between the accelerating effect of flow and the inhibiting effect of the nutrient load. The addition of fiber to a formula may alter this balance. By delaying absorption of nutrients, fiber may extend the length of small intestine exposed to nutrients and thereby trigger more intense inhibitory feedback. To determine whether the addition of fiber favors nutrient-triggered inhibition over flow-driven acceleration, we studied intestinal transit after perfusion of a low-residue enteral formula compared with a fiber-supplemented formula at two perfusion rates (50 or 100 mL/h for 2 h) into the duodenum of dogs each with both a duodenal and midgut fistula. With the low-residue formula, intestinal transit accelerated when the flow rate increased from 50 to 100 mL/h (P < 0.05). With the fiber-supplemented formula, however, intestinal transit was inhibited regardless of the flow rate. To determine whether the fiber-supplemented formula inhibited intestinal transit by displacing nutrients distally, we compared intestinal transit when the two formulas, delivered at 100 mL/h, were diverted completely at the midgut fistula. Intestinal transit of the fiber-supplemented formula increased by 400%, eliminating the difference in intestinal transit speed between the two formulas. We concluded that the fiber-supplemented formula slowed intestinal transit by intensifying inhibitory feedback from the distal gut.

Analysis of Variance↗
PubMed1997

Comparison of Vibrio cholerae O1 isolates by polymerase chain reaction fingerprinting and ribotyping.

The rRNA gene restriction patterns and the polymerase chain reaction (PCR) fingerprinting types of 53 Vibrio cholerae O1 isolates were studied. Five and eight patterns were observed from 27 toxigenic and 26 non-toxigenic O1 isolates after BglI cleavage. PCR fingerprinting with three primer sets aimed at enterobacterial repetitive intergenic consensus (ERIC) sequences, ERIC-related sequences in V. cholerae, another kind of repeated sequences in V. cholerae (VCR) and arbitrary sequences divided the same strains into seven and 10 PCR types, respectively. Eight ribotypes had unique PCR patterns. PCR fingerprinting identified more than one pattern among isolates within each of the remaining ribotypes. However, ribotyping was able to differentiate the same PCR types in one case. A single ribotype and a single PCR pattern were found in toxigenic O1 strains isolated in Taiwan from imported food and imported cases of cholera between 1993 and 1995. Typing of V. cholerae O1 by PCR fingerprinting correlated well with ribotyping, but was more discriminating. PCR assay provides a rapid and simple means of typing these strains for epidemiological studies.

Cholera↗
PubMed1997

Gall-bladder wall thickening in patients with liver cirrhosis.

Gall-bladder wall thickening is commonly seen in patients with cirrhosis, but its exact causes have not been well established. We evaluated clinical, biochemical and haemodynamic data of patients with cirrhosis with respect to the presence of thickening of the gall-bladder wall. After excluding patients who presented with gallstones, acute or chronic cholecystitis, heart failure, a serum creatinine level greater than 2 mg/dL and/or a serum alanine aminotransferase level greater than 400 U/L, 77 patients with cirrhosis (75 male, two female; mean age 58 +/- 8 years) were enrolled in the study. Clinical, biochemical, ultrasound and haemodynamic data were obtained in every patient. Forty-one (53%) of 77 patients with cirrhosis had gall-bladder wall thickening (> 4 mm). Compared with patients with a normal gall-bladder wall, patients with gall-bladder wall thickening had significantly lower serum albumin levels (3.6 +/- 0.6 vs 2.9 +/- 0.7 gm/dL, respectively; P < 0.05), a longer prothrombin time (13 +/- 6 vs 16 +/- 6 s, respectively; P < 0.05), more patients with Child-Pugh class C (6 vs 37%, respectively; P < 0.05) and more patients with ascites (8 vs 50%, respectively; P < 0.05). In addition, compared with patients with a normal gall-bladder wall, those patients with gall-bladder wall thickening had a higher hepatic venous pressure gradient (13.9 +/- 4.5 vs 17.1 +/- 4.1 mmHg, respectively; P < 0.01) and a lower systemic vascular resistance (SVR; 1144 +/- 332 vs 1010 +/- 318 dyn.s/cm5, respectively; P < 0.05). Using a multivariate analysis, the presence of ascites and SVR lower than 900 dyn.s/cm5 were independently correlated with the presence of gall-bladder wall thickening, while a hepatic vein pressure gradient greater than 10 mmHg had only a marginally significant association. The presence of ascites, decreased SVR and portal hypertension are related to the occurrence of gall-bladder wall thickening in patients with cirrhosis, indicating that the development of gall-bladder wall thickening may be multifactorial.

Ascites↗
PubMed1997

Prolonged bleeding time: a new clinical manifestation of hepatocellular carcinoma?

The association between prolonged bleeding time and hepatocellular carcinoma (HCC) has not been well studied. We investigated whether bleeding time is prolonged in cirrhotic patients with HCC and studied the role of clinical characteristics, tumour size, and laboratory data in predicting bleeding time prolongation. After excluding patients that presented with blood dyscrasia and uraemia, 58 cirrhotic patients with HCC, 106 cirrhotic patients without HCC, and 44 age-and sex-matched healthy subjects were included in the study. Bleeding time, imaging studies, clinical characteristics and biochemical data were obtained for every patient. Cirrhotic patients with and without HCC had longer bleeding times (554 +/- 32 s, respectively) compared with healthy controls (357 +/- 13 s, P < 0.05). Hepatocellular carcinoma patients with a large tumour burden (> 5 cm in diameter) had a significantly longer bleeding time than those patients without (663 +/- 105 vs 376 +/- 23 s, respectively, P < 0.05). After excluding patients with a platelet count < or = 80 000/mm3, cirrhotic patients classified as Child-Pugh's grading A and with a large tumour burden had longer bleeding times(580 +/- 87 s) than patients with a small tumour burden (< or = 5cm in diameter) and cirrhotic patients without HCC (371 +/- 22 and 416 +/- 29 s, respectively, P < 0.05). In cirrhotic patients with HCC, higher serum bilirubin levels, a Child-Pugh's grading C, and a tumour size > 5 cm in diameter were found to be significant predictors for prolonged bleeding time on univariate analysis. On multivariate analysis, both tumour size > 5 cm in diameter and a Child-Pugh's grading C (odd's ratio, 95% confidence interval and P value were measured as 38.5, 2.8-534.7, < 0.001, and 10.5, 0.9-117.6, 0.02, respectively) were the significant independent predictors. A significant correlation existed between tumour diameter and bleeding time (r = 0.44, P < 0.01). In conclusion, these results suggest that prolonged bleeding time may be categorized as a new clinical manifestation in patients with HCC. In addition to cirrhosis, HCC itself may also participate in the pathogenesis of bleeding time prolongation.

Bleeding Time↗
PubMed1997

Haemodynamic effects of chronic tetrandrine treatment in portal hypertensive rats.

Tetrandrine is a calcium channel antagonist with reported antihypertensive effect. However, the potential role of tetrandrine as a therapeutic agent in portal hypertension has yet to be explored. The present study aimed to investigate the haemodynamic effects of chronic tetrandrine treatment on portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Animals were allocated into one of two groups: a tetrandrine group and a vehicle group. Tetrandrine (20 mg/kg) or vehicle was administered by gavage every 12 h for 8 consecutive days, starting 1 day before ligation and continuing thereafter. After 8 days of tetrandrine treatment, systemic haemodynamics, organ blood flow and the degree of portal-systemic shunting were measured after an overnight fast. The portal venous pressure and protal tributary blood flow were significantly decreased, while portal territory as well as hepto-collateral vascular resistance significantly increased in the tetrandrine group compared with the vehicle group. The cardiac index was increased, while systemic vascular resistance was decreased, the the tetrandrine group. Mean arterial pressure, heart rate, portal-systemic shunting and bodyweight were similar between the two groups. Renal blood flow was decreased in the tetrandrine group. In conclusion, long-term treatment of tetrandrine reduced portal venous pressure and alleviated splanchnic hyperaemina in portal hypertensive rats without affecting the portal-systemic shunting.

Alkaloids↗
PubMed1997

Portal hypotensive effects of tetrandrine and verapamil in portal hypertensive rats.

The portal hypotensive effects of tetrandrine and verapamil (both calcium-channel blockers) were assessed in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Both tetrandrine (4, 8, 16 and 24 mg kg-1) and verapamil (0.5, 1.0, 1.5 and 2.0 mg kg-1) induced dose-dependent decreases of portal venous pressure and mean arterial pressure after intravenous infusion. for example, infusion of tetrandrine (16 mg kg-1) induced a maximum reduction of portal venous pressure and mean arterial pressure approximately 1 min after the start of infusion. Portal venous pressure decreased from baseline (12.5 mmHg) to 10.0 mmHg, and mean arterial pressure from baseline (90 mmHg) to 80 mmHg. Heart rate decreased from 250 to 240 beats min-1. At 24 mg kg-1, tetrandrine reduced portal venous pressure and mean arterial pressure to 20.3 +/- 2.4% and 28.4 +/- 1.4% of baseline, respectively. Our results show that both tetrandrine and verapamil induce portal pressure reduction in portal hypertensive animals.

Alkaloids↗